Monocytes in HIV associated atherosclerosis: A review of pathogenesis and clinical implications.

Atherosclerosis, a chronic inflammatory disease of arterial walls, remains a leading cause of global mortality, with ischemic heart disease (IHD) and stroke as primary contributors. In people living with HIV (PLWH), this risk is amplified due to persistent immune activation and conventional cardiovascular risk factors such as hypertension and dyslipidemia. HIV-specific mechanisms, including viral proteins, gut microbial translocation, and chronic inflammation, drive monocyte dysfunction, foam cell formation, and vascular damage, contributing to accelerated atherogenesis. Antiretroviral therapy (ART) has significantly improved the life expectancy of PLWH, transforming HIV into a chronic condition. However, ART does not fully normalize immune activation, particularly monocyte-driven inflammation, which remains central to atherosclerosis progression. Protease inhibitor (PI)-based ART regimens are associated with metabolic disturbances, exacerbating dyslipidemia and insulin resistance, further increasing cardiovascular disease (CVD) risk. Imaging techniques, such as carotid intima-media thickness (CIMT) and coronary artery calcium (CAC) scoring, reveal subclinical atherosclerosis in this population. Adjunctive therapies like statins and anti-inflammatory agents, including interleukin (IL)-1β antagonists, show promise in mitigating inflammation and CVD risk. Targeted strategies addressing monocyte activation, chronic inflammation, and gut microbial translocation are critical. Comprehensive care for PLWH requires integrating ART optimization with lifestyle interventions, lipid-lowering therapies, and novel treatments targeting immune dysfunction. Future research should refine biomarkers for early atherosclerosis detection, tailor CVD risk assessments, and explore therapeutic innovations to reduce cardiovascular morbidity and mortality in PLWH.